Noradrenergic Control of Thalamic Oscillation: the Role of α‐2 Receptors
- 1 March 1991
- journal article
- Published by Wiley in European Journal of Neuroscience
- Vol. 3 (3) , 222-229
- https://doi.org/10.1111/j.1460-9568.1991.tb00083.x
Abstract
The effects of α-adrenergic drugs on neocortical high voltage spike and wave spindles (HVS), reflecting thalamic oscillation, was investigated in freely moving rats. HVS occurred spontaneously in the awake but immobile animal. Peripheral administration of the α-1 antagonist, prazosin and α-2 agonists, xylazine and clonidine increased the incidence and duration of HVS in a dose-dependent manner. The α-2 antagonist, yohimbine and the tricyclic antidepressants, desipramine and amitriptyline, significantly decreased the incidence of the neocortical HVS. Bilateral microinjections of the α-2 agonists into the nucleus ventralis lateralis area of the thalamus, but not into the hippocampus or corpus callosum, was as effective as peripheral injection of these drugs. Xylazine was most effective in Fischer 344 rats that display high spontaneous rate of HVS and less effective in the Sprague – Dawley and Buffalo strains. The HVS-promoting effect of clonidine was antagonized by prior intrathalamic injection of the α-2 antagonist, yohimbine. The amplitude of the HVS was increased by picomole amounts of unilaterally-injected clonidine. Neurotoxic destruction of the thalamopetal noradrenergic afferents by intracisternal or intrathalamic injection of 6-hydroxydopamine, but not by peripheral administration of DSP-4, increased the incidence of HVS. Importantly, intrathalamic administration of xylazine continued to induce HVS after destroying the thalamic noradrenergic terminals. Following downregulation of the α-2 adrenoceptors by chronic administration (3 weeks) of amitriptylene the incidence of HVS decreased and the effectiveness of intrathalamic xylazine on the induction of HVS was significantly reduced. Based on these findings, we suggest that a major action of α-2 adrenergic drugs on thalamic oscillation may be mediated by postsynaptic α-2 adrenoceptors located on the thalamocortical neurons. We hypothesize that noradrenaline in the thalamus has a dual effect on the relay cells: blocking and promoting thalamic oscillation via α-1 and α-2 receptors, respectively. The final physiological effect is assumed to be a function of the relative density and affinity of these adrenergic receptor subtypes.Keywords
This publication has 49 references indexed in Scilit:
- Three types of neuronal calcium channel with different calcium agonist sensitivityNature, 1985
- Sleep and EpilepsyEpilepsia, 1985
- The epileptic nature of rodent electrocortical polyspiking is still unprovenExperimental Neurology, 1985
- Spontaneous EEG Paroxysms in the Rat: Effects of Psychotropic and Alpha-Adrenergic AgentsNeuropsychobiology, 1985
- A low voltage-activated, fully inactivating Ca channel in vertebrate sensory neuronesNature, 1984
- Enhancement of spike and wave discharges by GABAmimetic drugs in rats with spontaneous petit-mallike epilepsyNeuroscience Letters, 1984
- α2-adrenergic antagonists suppress epileptiform EEG activity in a seizure modelLife Sciences, 1982
- Functional evidence for subsensitivity of noradrenergic α2 receptors after chronic desipramine treatmentLife Sciences, 1980
- Presynaptic receptors and the control of noradreneline releaseTrends in Pharmacological Sciences, 1980
- Inherited Epilepsy: Spike-Wave and Focal Motor Seizures in the Mutant Mouse TotteringScience, 1979